Ranking the role of RANK ligand in apoptosis

被引:41
作者
Bharti, AC
Aggarwal, BB
机构
[1] Univ Texas, MD Anderson Canc Ctr, Cytokine Res Sect, Dept Expt Therapeut, Houston, TX 77030 USA
[2] ICMR, Inst Cytol & Prevent Oncol, Noida, Uttar Pradesh, India
关键词
Akt; apoptosis; cell cycle arrest; JNK; NF-kappa B; PI3Kinase; RANK; RANKL; TRAF6;
D O I
10.1023/B:APPT.0000045780.10463.c6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Many members of tumor necrosis factor (TNF) superfamily are characterized by their ability to induce apoptosis once they bind in a homotrimeric manner to their cognate receptors. The receptor activator of nuclear factor-kappaB ligand (RANKL), a member of the TNF superfamily identified seven years ago, was originally described as a factor that induced osteoclastogenesis and dendritic cell survival. Recent observations indicate that a growth inhibitory and apoptosis-inducing activity is associated with RANKL, as is the case for other members of TNF superfamily. This review describes the possible mechanisms of induction of RANKL-induced growth inhibition/apoptosis and discusses the role of various components in RANKL-signaling in this phenomenon, including TNF receptor-associated factor (TRAF)-6, nuclear factor-kappaB (NF-kappaB), c-jun N-terminal kinase JNK), phosphatidylinositol-3 kinase (PI3K).
引用
收藏
页码:677 / 690
页数:14
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